IL10RB Knockout HAP1 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population derived from the HAP1 cell line, featuring targeted disruption of the IL10RB gene. IL10RB encodes the shared beta subunit (IL-10R??) of the interleukin-10 receptor family, which includes functional receptors for IL-10, IL-22, IL-26, IL-28, and IL-29. The polyclonal format offers a heterogeneous pool of gene-edited cells, enabling broad functional interrogation in a near-haploid genetic background. This ready-to-use knockout model eliminates the need for researchers to perform independent gene editing, accelerating mechanistic studies and screening campaigns.
HAP1 is a near-haploid human cell line originally derived from a male patient with chronic myelogenous leukemia (CML). It retains expression of the BCR-ABL1 fusion oncogene, characteristic of CML, and remains a widely used hematopoietic and leukemic model. The near-haploid karyotype simplifies genetic manipulation and reduces the complexity of downstream genotypic and phenotypic analyses, as target gene disruption typically requires editing only one allele.
IL10RB functions as an essential shared co-receptor that pairs with distinct alpha chains??IL10RA, IL22RA1, and IL28RA??to assemble signaling-competent heterodimeric receptor complexes. Upon ligand engagement, IL10RB recruits JAK1 and TYK2 kinases, which phosphorylate and activate STAT3. Activated STAT3 dimers translocate to the nucleus to drive transcription of target genes such as SOCS3 and IL1RN, mediating anti-inflammatory and immunoregulatory responses. Through these interactions, IL10RB integrates signals from cytokines including IL-10, IL-22, IL-26, IL-28A, IL-28B, and IL-29 to control expression of immune-modulatory factors.
In the HAP1 leukemic context, disruption of IL10RB provides a platform to examine how IL-10 family cytokine signaling intersects with oncogenic pathways driven by BCR-ABL1. The model permits dissection of the JAK-STAT cascade in a hematopoietic lineage without confounding from a diploid genome, facilitating clean interpretation of signaling defects. Researchers can simulate chronic inflammatory cues and assess the dependency of leukemic cell behavior on IL10RB-mediated circuits. This system is particularly relevant for exploring links between inflammation and oncogenesis, and for validating therapeutic targets in inflammatory bowel disease, rheumatoid arthritis, psoriasis, and systemic lupus erythematosus.
Typical applications include cytokine stimulation assays followed by western blotting for STAT3 phosphorylation, RT-qPCR for SOCS3 induction, and flow cytometry for receptor surface expression analysis. The polyclonal knockout cells are also suitable for global transcriptional profiling by RNA-seq, enabling genome-wide interrogation of signaling networks. These applications support genetic interaction screens, drug target validation, and dissection of immunomodulatory compound mechanisms. For detailed product specifications and technical support, please contact Ascent Research.
